Article

CD40-CD40L interactions in atherosclerosis

Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands.
Trends in Cardiovascular Medicine (Impact Factor: 2.07). 02/2002; 12(1):27-32. DOI: 10.1016/S1050-1738(01)00142-6
Source: PubMed

ABSTRACT Increasing evidence supports a central role for CD40-CD40L interactions in the pathogenesis of atherosclerosis. Recently, we have shown that CD40L deficiency as well as pharmacological inhibition of CD40L in ApoE(-/-) mice results in the development of a stable atherosclerotic plaque phenotype. This phenotype is rich in smooth muscle cells and collagen, and contains only a small amount of macrophages and T-lymphocytes. CD40 and CD40L protein are present in almost all cell types in human atherosclerotic lesions. Expression was observed in early plaques, but was more predominant in advanced, rupture-prone, and ruptured plaques. Because most of the acute complications of atherosclerosis are the result of plaque rupture, CD40L inhibition might be a novel therapeutic approach to prevent atherosclerotic plaque destabilization and plaque rupture.

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